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LncRNA changes in the livers of db/db mice than that of C57 mice

ABSTRACT: lncRNA changes in the livers of db/db mice than that of C57 mice

PROVIDER: PRJNA419962 | ENA |

REPOSITORIES: ENA

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lncRNA changes in the livers of db/db mice than that of C57 mice

Project description:To identify putative lncRNA changes in the livers of db/db mice and C57 mice, we isolated the liver tissues and carried out a microarray analysis. Here, we found significant changes of lncRNAs in the livers of db/db mice. Among them, abnormal expression of ultraconserved elements was noticed.

2017-12-14 | GSE107396 | GEO

Examination of glycan-related gene expression in the livers of three groups of mice: wild-type, ad-lib-fed type 2 diabetic mice (db/db), and calorically restricted db/db mice

Project description:Assembly of HSPGs in the liver is defective in diabetes mellitus. A major consequence is impaired clearance of post-prandial lipoproteins, which ordinarily depends on the binding of these particles to hepatic HSPGs. Impaired clearance leads to prolonged exposure of the arterial wall to these harmful lipoproteins. We pin-pointed suppression of NDST-1 in livers of type 1 diabetic rats as at least a partial explanation for defective HSPG assembly. Dr. Williams' lab examined glycan-related gene expression in the livers of three groups of mice: wild-type, ad-lib-fed type 2 diabetic mice (db/db), and calorically restricted db/db mice (caloric restriction was shown several years ago to correct their clearance of atherogenic post-prandial lipoproteins). The results will indicate the molecular basis for defective HSPG assembly in type 2 diabetes, which is a question of considerable medical importance. RNA preparations from mice livers (wild-type, ad-lib-fed type 2 diabetic mice, and calorically restricted mice) were sent to Microarray Core (E). The RNA was amplified, labeled, and hybridized to GLYCO_v3 microarrays.

2011-04-29 | E-GEOD-28938 | biostudies-arrayexpress

microRNA microarray profiling in the livers of control db/+ and diabetic db/db mice

Project description:Analysis revealed a set of 13 microRNAs to be significantly altered between livers of control db/+ and diabetic db/db mice. Of these, miR-34a, miR-107, miR-378, miR-378*, miR-31, miR-31*, miR-151-5p, miR-676, miR-22, miR-93, let-7b were up-regulated and let-7e and miR-227 were down-regulated. A total of 670 predicted targets for these altered miRNAs were extracted from PicTar and TargetScan and functional characterisation mapped these targets to several biological processess related to varied metabolic pathways. The Wnt signaling pathway that has been shown to be linked to diabetes emerged as the most prominent pathway from these sets of target genes.

2011-12-22 | GSE17035 | GEO

Transcription profiling of the effect of metformin (50mg/kg,400mg/kg) on gene expression in livers of db/db mice

Project description:Effect of metformin (50mg/kg,400mg/kg) on gene expression in livers of db/db mice.

2006-11-18 | E-MEXP-490 | biostudies-arrayexpress

Expression data from livers of F2 mice (C57BL/6 X DBA/2) deficient in leptin receptor (db/db)

2011-12-29 | GSE30140 | GEO

Expression data from livers of F2 mice (B57BL/6 X DBA/2) deficient in leptin receptor (db/db)

Project description:In several models of obesity-induced diabetes, increased lipid accumulation in the liver has been associated with decreased diabetes susceptibility. For instance, deficiency in leptin receptor (db/db) leads to hyperphagia and obesity in both C57BL/6 and C57BLKS mice but, only on the C57BLKS background do the mice develop beta-cell loss leading to severe diabetes while C57BL/6 mice are relatively resistant. Liver triglyceride levels in the resistant C57BL/6 mice are 3 to 4 fold higher than in C57BLKS. To better understand the mechanisms contributing to metabolic dysfunction in obesity-induced diabetes, we used microarrays to comprehensively profile gene expression livers of F2 mice (B57BL/6 X DBA/2) deficient in leptin receptor (db/db) DBA/2J females were mated to C57BL/6 males carrying leptin receptor deficiency (db/+) and, F1 (db/+) offspring were interbred to produce F2 mice. Offspring deficient in leptin receptor (db/db) were fed on a chow diet until 5 weeks or 12 weeks of age and then euthanized for collection of liver tissue for RNA profiling along with other diabetes-related phenotypes.

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Hepatic gene expression profiles of db/db mice with non-alcoholic fatty liver

Project description:Nonalcoholic fatty liver disease (NAFLD) is a common disorder in obese people and is becoming the leading cause of hepatocellular carcinoma (HCC). Recently, lncRNAs have been proven to play remarkable roles in numerous biological processes and human diseases, including NAFLD. However, the function of lncRNA in NAFLD pathogenesis remains largely unknown. The aim of this study was to explore the lncRNA expression profile in NAFLD mice and to identify novel lncRNAs involved in the pathogenesis of NAFLD. We performed microarray analysis to compare the expression profiles of lncRNAs and mRNAs in the liver of diabetic db/db mice with NAFLD and normal mice.

2017-12-19 | GSE108228 | GEO

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Profiling pancreatic islets from obese db/db and lean control db/+ mice

Project description:This program addresses the molecular basis of beta-cell failure associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in pancreatic islets of the db/db mice compared to the control db/+ mice? The db/db mice islets profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the islets of db/db mice compared to the corresponding db/+ controls.

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Next-generation sequencing facilitates quantitative analysis of wild type and diabetic db/db mice islets transcriptomes

Project description:Long non-coding RNAs (LncRNAs) constitute an extensive fraction of the mammalian transcriptome. In this study, lncRNAs dysregulated in the islets of diabetic db/db mice were identified by high-throughput RNA sequencing. More than 1600 lncRNAs were detected using RNA sequencing, indicating that lncRNAs were abundant in islets. Among them, we found that lncRNA-Malat1 was significantly reduced in diabetic mouse islets. Further experiments suggested an involvement of lncRNA-Malat1 in lipotoxicity-induced β-cell dysfunction.

2022-11-01 | GSE139823 | GEO

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